Overactivation of the NF-κB pathway impairs molar enamel formation

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Item Type:	Article
Title:	Overactivation of the NF-κB pathway impairs molar enamel formation
Creators Name:	Yamada, A., Kawasaki, M., Miake, Y., Yamada, Y., Blackburn, J., Kawasaki, K., Trakanant, S., Nagai, T., Nihara, J., Kudo, T., Meguro, F., Schmidt-Ullrich, R., Liu, B., Hu, Y., Page, A., Ramírez, Á., Sharpe, P.T., Maeda, T., Takagi, R. and Ohazama, A.
Abstract:	OBJECTIVE: Hypohidrotic ectodermal dysplasia (HED) is a hereditary disorder characterized by abnormal structures and functions of the ectoderm-derived organs, including teeth. HED patients exhibit a variety of dental symptoms, such as hypodontia. Although disruption of the EDA/EDAR/EDARADD/NF-κB pathway is known to be responsible for HED, it remains unclear whether this pathway is involved in the process of enamel formation. EXPERIMENTAL SUBJECTS AND METHODS: To address this question, we examined the mice overexpressing Ikkβ (an essential component required for the activation of NF-κB pathway) under the keratin 5 promoter (K5-Ikkβ). RESULTS: Upregulation of the NF-κB pathway was confirmed in the ameloblasts of K5-Ikkβ mice. Premature abrasion was observed in the molars of K5-Ikkβ mice, which was accompanied by less mineralized enamel. However, no significant changes were observed in the enamel thickness and the pattern of enamel rods in K5-Ikkβ mice. Klk4 expression was significantly upregulated in the ameloblasts of K5-Ikkβ mice at the maturation stage, and the expression of its substrate, amelogenin, was remarkably reduced. This suggests that abnormal enamel observed in K5-Ikkβ mice was likely due to the compromised degradation of enamel protein at the maturation stage. CONCLUSION: Therefore, we could conclude that the overactivation of the NF-κB pathway impairs the process of amelogenesis.
Keywords:	Molar, Enamel, NF-κB, Tooth Development, Animals, Mice
Source:	Oral Diseases
ISSN:	1354-523X
Publisher:	Wiley
Volume:	26
Number:	7
Page Range:	1513-1522
Date:	October 2020
Official Publication:	https://doi.org/10.1111/odi.13384
PubMed:	View item in PubMed

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